Electrophysiological remodeling in heart failure

Abstract

Ion channel remodeling in heart failure modulates key cellular electrophysiological properties, predisposing to arrhythmias and sudden death. Heart failure induced ion channel dysfunction prolongs the action potential, increases spatio-temporal gradients of repolarization, promotes arrhythmogenic triggers and results in conduction abnormalities. Understanding fundamental ionic mechanisms of normal and abnormal electrogenesis is a key requirement for the development of effective and safe therapies. Elucidating the underlying molecular mechanisms and functional consequences of ion channel remodeling at the cellular and organ levels presents a unique opportunity for the development of novel pharmacological, device, gene, and cell based approaches for the treatment of arrhythmias in heart failure.